High impact information on LCOR

• Receptor interacting protein 140 (RIP140), a ligand-dependent corepressor for nuclear receptors, can be modified by arginine methylation [1].
• Previously we have shown that the ligand-dependent corepressor, RIP140, is a direct transcriptional target of all-trans retinoic acid (RA) [2].
• Unexpectedly, the mutant receptor silences basal gene transcription, recruits corepressors (the silencing mediator of retinoid and thyroid receptors and the nuclear corepressor) more avidly than wild-type PPARgamma, and exhibits delayed ligand-dependent corepressor release [3].
• The inhibition was not complement dependent, did not require the continuous presence of MLR2 in culture, and could not be detected also when human placenta-conditioned medium was used in the place of leukocyte feeder layers as a source of colony-stimulating factor (CSF) [4].
• A monoclonal antibody specifically reactive with MLR-activated T cells (MLR2) was added to light density normal marrow cells, depleted of adherent cells and T lymphocytes, and plated in soft agar for granulocyte macrophage colony formation [4].

Biological context of LCOR

• Both MLR1 and MLR2 partially blocked NGF induced cell death in a mouse cell-line that expresses p75NTR but not TrKA [5].
• Corepressors such as LCoR and RIP140 may function in negative feedback loops to attenuate hormone-induced transactivation, act more transiently as part of a cycle of cofactors recruited to target promoters by ligand-bound receptors, or function in hormone-induced target gene repression [6].

Anatomical context of LCOR

• Thus, MLR2 stains nearly all the responder T cells present in a secondary MLR, while MLR 1, 3 and 4 stain only a fraction [7].
• Importantly, intracerebroventricular injections indicated MLR2 was internalized within the cell bodies of mouse basal forebrain neurons, further demonstrating that this antibody is biologically active [5].
• Mlr1 was expressed predominantly in the spermatocytes of the testis, while Mlr2 was expressed in various tissues other than testis [8].
• None of the cortical and spinal latencies (Lcor and Lsp, respectively) and the central motor conduction time were different between MES and PES in the upper limb muscles [9].

Physical interactions of LCOR

• Thus, these structural analyses provide mechanistic insight into the etiology of RTH disease in human TRbeta mutants that exhibit hormone binding with decreased ligand-dependent corepressor release [10].

Analytical, diagnostic and therapeutic context of LCOR

• Co-culture experiments with MLR2 treated and untreated marrow cells further excluded the possibility of an indirect effect of MLR2 on CFU-c via auxiliary cells [4].
• MLR1 and MLR2 bound to human p75NTR with higher affinity than the well-characterized ME20.4 in ELISA and also recognized p75NTR present on neurons in both rat and mouse [5].

References